It is well recognised that hyperinflammation induced by SARS-CoV-2 is a major cause of disease severity and mortality in infected patients and many of the proposed treatments include agents currently used in rheumatologic clinical practice.1 One critical question, however, is which anti-inflammatory drugs are most appropriate. Among the most traditional non-biological anti-inflammatory therapies, corticosteroids appear to provide some benefit in advanced stages of the disease,2 but concerns may arise from immunosuppression induced during viral replicative phase. On the contrary, no data are available on possible effects of non-steroidal anti-inflammatory drugs (NSAIDs).

In their interesting paper,3 Reyes et al highlighted the potential anti-inflammatory role of colchicine in COVID-19. The primary mechanism of action of colchicine is tubulin disruption leading to down-regulation of multiple inflammatory pathways.4 Among these, colchicine is able to impair platelet aggregation and leucocyte migration through an action on adhesion molecules,5 effect shared with NSAIDs, including salicylates.6 7 However, another important anti-inflammatory effect of colchicine, not described for NSAIDs, derives from its ability to inhibit the NLR family pyrin domain containing 3

(NLRP3) inflammasome with consequent reduction of proinflammatory cytokines.4 It is for this reason that colchicine …